Interleukin-5 induces apoptotic defects in CD4+ T cells of patients with allergic rhinitis

Luo, Xiang‐Qian; Ma, Fei; Wang, Shuai; Zhao, Min; Shao, Jianbo; Geng, Xinyu; Liu, Jiang‐Qi; Mo, Li‐Hua; Guan, Li; Liu, Zhigang; Liu, Dabo; Yang, Ping‐Chang

doi:10.1002/jlb.3a0718-287rr

Cited by 10 publications

(11 citation statements)

References 21 publications

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“…The present data show that the low serum sCD83 levels are negatively correlated with the Th2 response in AR patients, suggesting that the low serum sCD83 levels are associated with the pathogenesis of Th2 polarization. Previous reports show that CD4 + T cells from patients with allergic diseases express high levels of Bcl2L12 [16,17], the present data also show that sTh2 cells express high Bcl2L12 levels. Bcl2L12 is an apoptosis inhibitor.…”

Section: Discussionsupporting

confidence: 84%

“…3A-E). Exposure of sTh2 cells to IL-5 [16] in the culture further increased Bcl2L12 expression in the cells (Fig. 3C-E).…”

Section: Serum Levels Of Scd83 Negatively Correlate With Bcl2l12 Exprmentioning

confidence: 84%

“…Published data indicate that IRF1 is the transcription factor of interferon (IFN)-γ and plays a critical role in triggering Th1 response [18], and Bcl2L12 contributes to Th2 polarization development [16,17]. Thus, we hypothesize that sCD83 may up regulate IRF1 expression to suppress Bcl2L12 expression in sTh2 cells.…”

Section: Scd83 Up Regulates Interferon Regulatory Factor 1 (Irf1) Expmentioning

confidence: 93%

“…Following our established procedures [16], AR responses were assessed in each mouse, including AR symptoms (sneezing and nasal scratching), serum levels of specific IgE and mouse mast cell protease-1 (mMCP1), Th2 cytokine amounts in nasal tissue protein extracts and nasal epithelial barrier permeability to FITC-dextran (Sigma Aldrich). (Levels of specific IgE, mMCP1, Th2 cytokines were assessed by ELISA following the manufacturer's instruction; the reagents were purchased from R&D Systems).…”

Section: Assessment Of Ar Response In Ar Micementioning

confidence: 99%

“…4G-H). The cells were then stimulated by IL-5 [16] in the culture in the presence or absence of sCD83. Exposure to IL-5 markedly increased the Bcl2L12 expression in sTh2 cells; the Bcl2L12 expression was suppressed by the presence of sCD83, that was abolished by the depletion of CD154 (Fig.…”

Section: Serum Levels Of Scd83 Negatively Correlate With Bcl2l12 Exprmentioning

confidence: 99%

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Soluble CD83 alleviates experimental allergic rhinitis through modulating antigen-specific Th2 cell property

Wu¹,

Song²,

Geng³

et al. 2020

Int. J. Biol. Sci.

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Background and aims: Dysfunction of the immune regulatory system plays a role in the pathogenesis of allergic rhinitis (AR). The underlying mechanism needs to be further investigated.Published data indicate that soluble CD83 (sCD83) has immune regulatory activities. This study aims to investigate the role of sCD83 in the alleviation of experimental AR. Methods: Peripheral blood samples were obtained from AR patients. Serum levels of sCD83 were determined by enzyme-linked immunosorbent assay. A murine AR model was developed to test the effects of sCD83 on suppressing experimental AR. Results: We found that serum levels of sCD83 in the AR group were lower than that in the healthy control group. A negative correlation was identified between the serum sCD83 levels and the frequency of T helper-2 (Th2) cells. The low serum sCD83 levels were also associated with the Bcl2L12 expression in antigen-specific Th2 cells. Exposure to sCD83 enhanced the responsiveness of antigen-specific Th2 cells to apoptosis inducers via suppressing the Bcl2L12 expression. Administration of sCD83 efficiently suppressed experimental AR. Conclusions: sCD83 contributes to immune homeostasis by regulating CD4 + T cell activities. Administration of sCD83 may have translational potential for the treatment of AR or other allergic diseases.

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Section: Discussionsupporting

confidence: 84%

“…3A-E). Exposure of sTh2 cells to IL-5 [16] in the culture further increased Bcl2L12 expression in the cells (Fig. 3C-E).…”

Section: Serum Levels Of Scd83 Negatively Correlate With Bcl2l12 Exprmentioning

confidence: 84%

Section: Scd83 Up Regulates Interferon Regulatory Factor 1 (Irf1) Expmentioning

confidence: 93%

Section: Assessment Of Ar Response In Ar Micementioning

confidence: 99%

Section: Serum Levels Of Scd83 Negatively Correlate With Bcl2l12 Exprmentioning

confidence: 99%

See 3 more Smart Citations

Soluble CD83 alleviates experimental allergic rhinitis through modulating antigen-specific Th2 cell property

Wu¹,

Song²,

Geng³

et al. 2020

Int. J. Biol. Sci.

Self Cite

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A20-OVA Nanoparticles Inhibit Allergic Asthma in a Murine Model

et al. 2020

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Mechanisms of Allergen Immunotherapy in Allergic Rhinitis

Drazdauskaité

Layhadi

Shamji

2020

Curr Allergy Asthma Rep

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Purpose of Review Allergic rhinitis (AR) is a chronic inflammatory immunoglobulin (Ig) E-mediated disease of the nasal mucosa that can be triggered by the inhalation of seasonal or perennial allergens. Typical symptoms include sneezing, rhinorrhea, nasal itching, nasal congestion and symptoms of allergic conjunctivitis. AR affects a quarter of the population in the United States of America and Europe. Recent Findings AR has been shown to reduce work productivity in 36–59% of the patients with 20% reporting deteriorated job attendance. Moreover, 42% of children with AR report reduced at-school productivity and lower grades. Most importantly, AR impacts the patient’s quality of life, due to sleep deprivation. However, a proportion of patients fails to respond to conventional medication and opts for the allergen immunotherapy (AIT), which currently is the only disease-modifying therapeutic option. AIT can be administered by either subcutaneous (SCIT) or sublingual (SLIT) route. Both routes of administration are safe, effective, and can lead to tolerance lasting years after treatment cessation. Both innate and adaptive immune responses that contribute to allergic inflammation are suppressed by AIT. Innate responses are ameliorated by reducing local mast cell, basophil, eosinophil, and circulating group 2 innate lymphoid cell frequencies which is accompanied by decreased basophil sensitivity. Induction of allergen-specific blocking antibodies, immunosuppressive cytokines, and regulatory T and B cell phenotypes are key pro-tolerogenic adaptive immune responses. Conclusion A comprehensive understanding of these mechanisms is necessary for optimal selection of AIT-responsive patients and monitoring treatment efficacy. Moreover, it could inspire novel and more efficient AIT approaches.

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Interleukin-5 induces apoptotic defects in CD4+ T cells of patients with allergic rhinitis

Cited by 10 publications

References 21 publications

Soluble CD83 alleviates experimental allergic rhinitis through modulating antigen-specific Th2 cell property

Soluble CD83 alleviates experimental allergic rhinitis through modulating antigen-specific Th2 cell property

A20-OVA Nanoparticles Inhibit Allergic Asthma in a Murine Model

Mechanisms of Allergen Immunotherapy in Allergic Rhinitis

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